Gut microbiota affects the estrus return of sows by regulating the metabolism of sex steroid hormones

Background Sex hormones play important roles in the estrus return of post-weaning sows.Previous studies have demonstrated a complex and bi-directional regulation between sex hormones and gut microbiota.However,the extent to which the gut microbiota affects estrus return of post-weaning sows is largely unknown.Results In this study,we first screened 207 fecal samples from well-phenotyped sows by 16S rRNA gene sequencing and identified significant associations between microbes and estrus return of post-weaning sows.Using metagenomic sequencing data from 85 fecal samples,we identified 37 bacterial species that were significantly associated with estrus return.Normally returning sows were characterized by increased abundances of L.reuteri and P.copri and decreased abundances of B.fragilis,S.suis,and B.pseudolongum.The changes in gut microbial composition significantly altered the functional capacity of steroid hormone biosynthesis in the gut microbiome.The results were confirmed in a validation cohort.Significant changes in sex steroid hormones and related compounds were found between normal and non-return sows via metabolome analysis.An integrated analysis of differential bacterial species,metagenome,and fecal metabolome provided evidence that normal return-associated bacterial species L.reuteri and Prevotella spp.participated in the degradation of pregnenolone,progesterone,and testosterone,thereby promoting estrogen biosynthesis.Furthermore,the microbial metabolites related to sow energy and nutrient supply or metabolic disorders also showed relationships with sow estrus return.Conclusions An integrated analysis of differentially abundant bacterial species,metagenome,and fecal metabolome revealed the involvement of L.reuteri and Prevotella spp.in sow estrus return.These findings provide deep insight into the role of gut microbiota in the estrus return of post-weaning sows and the complex cross-talk between gut microbiota and sex hormones,suggesting that the manipulation of the gut microbiota could be an effective strategy to improve sow estrus return after weaning.

Effect of Aldicarb Exposure on Cellular Immunity and Antioxidant Capacity in Kun-ming Mice

Immune function and antioxidant defense play an important role in protecting animals against pathogens and in controlling oxidative stress, respectively. Aldicarb is of great concern for human health due to its toxic nature, its extensive usage and consequent pollution. The hypothesis that aldicarb exposure would suppress immune function and antioxidant capacity in Kunming mice was to be tested in the present study. Twenty-three adult male mice were randomly divided into the control (n = 11) and the aldicarb treated (n = 12) groups. Food and water were provided ad libtum for both groups, while the aldicarb treated mice drank aldicarb solution (0.097 mg/L) for 22 days. Cellular immunity assessed by phytohaemagglutinin (PHA) response did not differ between the control and the aldicarb treated groups. Similarly, white blood cells were not influenced by aldicarb treatment. Moreover, aldicarb exposure had not significant effect on body mass, all organ masses detected. However, aldicarb treatment suppressed total antioxidant capacity in liver but not in kidneys. In summary, aldicarb treatment did not affect immune function, but suppressed liver antioxidant capacity in Kunming mice.

AFF3-DNA methylation interplay in maintaining the mono-allelic expression pattern of XIST in terminally differentiated cells

X chromosome inactivation and genomic imprinting are two classic epigenetic regulatory processes that cause mono-allelic gene expression.In female mammals,mono-allelic expression of the long non-coding RNA gene X-inactive specific transcript(XIST)is essential for initiation of X chromosome inactivation upon differentiation.We have previously demonstrated that the central factor of super elongation complex-like 3(SEC-L3),AFF3,is enriched at gamete differentially methylated regions(DMRs)of the imprinted loci and regulates the imprinted gene expression.Here,we found that AFF3 can also bind to the DMR downstream of the XIST promoter.Knockdown of AFF3 leads to de-repression of the inactive allele of X IST in terminally differentiated cells.In addition,the binding of AFF3 to the XIST DMR relies on DNA methylation and also regulates DNA methylation level at DMR region.However,the KAP1-H3K9 methylation machineries,which regulate the imprinted loci,might not play major roles in maintaining the mono-aUelic expression pattern of XIST in these cells.Thus,our results suggest that the differential mechanisms involved in the X IST DMR and gDMR regulation,which both require AFF3 and DNA methylation.